Journal article
CpG DNA: immunomodulation and remodelling of the asthmatic airway
Expert opinion on biological therapy, Vol.4(9), pp.1533-1540
09/01/2004
DOI: 10.1517/14712598.4.9.1533
PMID: 15335319
Abstract
Asthma is a disorder of increasing severity and prevalence. Present understanding of the pathogenesis of asthma emphasises its inflammatory nature. Unbridled inflammation appears to induce irreversible changes, collectively known as airway remodelling. CpG oligonucleotides are a class of compounds that have been developed from studies of prokaryotic DNA. Bacterial DNA, for example, contains sequence motifs based on the dinucleotides cytosine-guanine (CpG); these motifs are suppressed in mammalian DNA and induce (as part of the innate immune system) inflammation, characterised by the induction of T helper type 1 and regulatory responses. The pattern of inflammation promoted by CpG DNA tends to suppress the cytokine and cellular responses characteristic of asthma and atopic disorders. This has led to the investigation and development of CpG DNA as a novel therapeutic approach for the treatment and prevention of these disorders. In addition to suppressing acute and persistent airway inflammation, CpG DNA also reduces the development of subepithelial collagen deposition, goblet cell hyperplasia/metaplasia, and other aspects of airway remodelling. In this paper, the effects of CpG DNA on asthma inflammation and remodelling are reviewed.
Details
- Title: Subtitle
- CpG DNA: immunomodulation and remodelling of the asthmatic airway
- Creators
- Vipul V JainJoel N Kline
- Resource Type
- Journal article
- Publication Details
- Expert opinion on biological therapy, Vol.4(9), pp.1533-1540
- Publisher
- Taylor & Francis
- DOI
- 10.1517/14712598.4.9.1533
- PMID
- 15335319
- ISSN
- 1471-2598
- eISSN
- 1744-7682
- Language
- English
- Date published
- 09/01/2004
- Academic Unit
- Pulmonary, Critical Care, and Occupational Medicine; Occupational and Environmental Health; Internal Medicine
- Record Identifier
- 9984094499002771
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